The skin is an important organ for homeostasis and host defense against foreign invaders. Specifically, it acts as the body's first line of defense against infection. Accordingly, it is important that lesions or wounds in the skin be rapidly closed to prevent infection. Some types of wounds, however, are resistant to healing under normal physiological conditions.
The process of wound healing involves a complex system of local and remote (systemic) resources. For example, amino acids and sugars are needed as substrates for collagen and proteoglycan synthesis. Migration of fibroblasts and epithelial/endothelial cells during the wound healing process places additional systemic demands on a subject during the wound healing process. Wounded tissues have unique nutritional needs and physiological features. Lymphocyte participation in wound healing has been demonstrated. Alteration in the hosts T-cell dependent immune response has also been shown to influence wound healing. Cyclosporine and anti T-cell antibodies, both of which interfere with T-cell function, abrogate wound healing. Similarly, macrophages and their products are also involved in wound healing. Increased circulation usually results in rapid delivery of monocytes and PMN's to the wound site. This in turn results in the elimination of bacterial contamination of the wound due to nonspecific killing mechanisms and also enhances the rate of wound healing. These various cell types are synthesized by the bone marrow.
While wound healing is typically an efficient and natural process that normally requires no special treatment, chronic non-healing wounds can occur. In the chronic cases, there is some underlying factor preventing healing and intervention is often necessary to complete the healing process. For example, pressure sores are initially acute wounds caused by ischaemic death of tissue due to excessive pressure and will usually heal readily when pressure is relieved and the blood supply restored. Often times it is difficult to resolve these causative factors and chronic wounds can develop. Most of these chronic wounds are characterized by the accumulation of devitalized tissue and cellular exudates at the outer surface. These products result from a restriction of nutrients to the damaged epithelium and form either a dry, hard eschar or, as in the case of deep moist wounds, a slough that frequently hardens on the outside with exposure to the air. The accumulation of these products in the wound bed is generally regarded to prevent or delay granulation and epithelialisation. The removal of this tissue by a process termed debridement is therefore thought to facilitate healing.
Debridement can be accomplished by both mechanical and non-mechanical methods. The mechanical methods require the physical elimination of the devitalized tissue from the healthy, but this difficult and often results in the aggravation of the wound. There are various non-mechanical debridement methods that include enzymes, hydrogels and chemical formulations. While various methods of debridement exist, there is no proven reliability of any particular method of debridement with respect to a particular wound. In particular, use of proteolytic enzymes in the early debridment (digestion and separation) of eschar tissues, such as in burn wounds, decubitus ulcers, pressure necroses and bed sores has been researched, e.g., streptokinase, trypsin and papain.
There remains a need for isolating and providing an agent that acts as an effective promoter of wound healing.